ReviewHypoxia (Auckland, N.Z.)2014
Macrophage-mediated response to hypoxia in disease.
Review in Hypoxia (Auckland, N.Z.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- Interplay of trauma-triggered auto-inflammation and T-cell auto-reactivity in posttraumatic dystrophy.Frontiers in immunology · 2025Review
- Acute hypoxia modulate macrophage phenotype accompanied with transcriptome re-programming and metabolic re-modeling.Frontiers in immunology · 2025Article
- The complex role of macrophages in pancreatic cancer tumor microenvironment: a review on cancer progression and potential therapeutic targets.Discover oncology · 2024Review
- TLR4 Agonist and Hypoxia Synergistically Promote the Formation of TLR4/NF-Analytical cellular pathology (Amsterdam) · 2022Article
- Characterization of atherosclerotic plaques in blood vessels with low oxygenated blood and blood pressure (Pulmonary trunk): role of growth differentiation factor-15 (GDF-15).BMC cardiovascular disorders · 2021Article
- Rationale for hyperbaric oxygen therapy in traumatic injury and wound care in small animal veterinary practice.The Journal of small animal practice · 2021Review
- Tumor-Associated Macrophages as Multifaceted Regulators of Breast Tumor Growth.International journal of molecular sciences · 2021Review
- Chemokine receptor 5 blockade modulates macrophage trafficking in renal ischaemic-reperfusion injury.Journal of cellular and molecular medicine · 2020Article
- Transportable system enabling multiple irradiation studies under simultaneous hypoxia in vitro.Radiation oncology (London, England) · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia plays a critical role in the pathobiology of various inflamed, diseased tissues, including malignant tumors, atherosclerotic plaques, myocardial infarcts, the synovia of rheumatoid arthritic joints, healing wounds, and sites of bacterial infection. These areas of hypoxia form when the blood supply is occluded and/or the oxygen supply is unable to keep pace with cell growth and/or infiltration of inflammatory cells. Macrophages are ubiquitous in all tissues of the body and exhibit great plasticity, allowing them to perform divergent functions, including, among others, patrolling tissue, combating invading pathogens and tumor cells, orchestrating wound healing, and restoring homeostasis after an inflammatory response. The number of tissue macrophages increases markedly with the onset and progression of many pathological states, with many macrophages accumulating in avascular and necrotic areas, where they are exposed to hypoxia. Recent studies show that these highly versatile cells then respond rapidly to the hypoxia present by altering their expression of a wide array of genes. Here we review the evidence for hypoxia-driven macrophage inflammatory responses in various disease states, and how this influences disease progression and treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.